The human T-lymphotropic virus or human T-cell lymphotropic virus (HTLV) family of viruses are a group of humanretroviruses that are known to cause a type of cancer called adult T-cell leukemia/lymphoma and a demyelinating disease called HTLV-I associated myelopathy/tropical spastic paraparesis (HAM/TSP). The HTLVs belong to a larger group of primate T-lymphotropic viruses (PTLVs). Members of this family that infect humans are called HTLVs, and the ones that infect old world monkeys are called Simian T-lymphotropic viruses (STLVs). To date, four types of HTLVs (human T-lymphotropic virus 1 [HTLV-I], human T-lymphotropic virus 2 [HTLV-II], HTLV-III, and HTLV-IV) and four types of STLVs (STLV-I, STLV-II, STLV-III, and STLV-V) have been identified. The HTLVs are believed to originate from intraspecies transmission of STLVs. The original name for HIV, the virus that causes AIDS, was HTLV-III; this term is no longer in use [1]. The HTLV-1 genome is diploid, composed of two copies of a single-stranded RNA virus whose genome is copied into a double-stranded DNA form that integrates into the host cell genome, at which point the virus is referred to as a provirus. A closely related virus is bovine leukemia virusBLV.

HTLV-II[edit]

A virus closely related to HTLV-I, also discovered by Robert Gallo and colleagues,[3] HTLV-II shares approximately 70% genomic homology (structural similarity) with HTLV-I.

HTLV-III and HTLV-IV[edit]

When HIV, the virus that causes AIDS, was characterized in 1984 by Robert Gallo,[4] he named it HTLV-III. HTLV-III is currently the name used to describe another virus related to HTLV-I and HTLV-II.[citation needed] "HTLV-IV" has been used to describe recently characterized viruses.[5][6][7]

These viruses were discovered in 2005 in rural Cameroon, and were, it is presumed, transmitted from monkeys to hunters of monkeys through bites and scratches.

HTLV-III is similar to STLV-III (Simian T-lymphotropic virus 3).[8] Multiple strains have been identified.[9] It expresses gag, pol, and env, among other proteins.[10]

HTLV-IV does not resemble any known virus.

It is not yet known how much further transmission has occurred among humans, or whether the viruses can cause disease.

The use of these names can cause some confusion, because the name HTLV-III was one of the names for HIV in early AIDS literature, but has since fallen out of use.[11] The name HTLV-IV has also been used to describe HIV-2.[12] A large Canadian study documented this confusion among healthcare workers, where >90% of HTLV tests ordered by physicians were actually intended to be HIV tests.[13]

Transmission[edit]

HTLV-I and HTLV-II are sexually transmitted.[14][15] Breast feeding by the carrier mother may cause vertical transmission.[16]

Research[edit]

While there is no present licensed vaccine, there are many factors which make a vaccine against HTLV-1 feasible. The virus displays relatively low antibody production variability, natural immunity does occur in humans, and experimental vaccination using envelope antigens has been shown to be successful in animal models. Four HTLVs are well established. HTLV-1 and HTLV-2 are both involved in actively spreading epidemics, affecting 15-20 million people worldwide. HTLV-1 is the more clinically significant of the two, as it has been proven to be the etiologic agent of multiple disorders. At least 500,000 of the individuals infected with HTLV-1 eventually develop an often rapidly fatal leukemia, while others will develop a debilitative myelopathy, and yet others will experience uveitis, infectious dermatitis, or another inflammatory disorder. HTLV-2 is associated with milder neurologic disorders and chronic pulmonary infections. The novel HTLV-3 and HTLV-4 have been isolated only in a few cases; no specific illnesses have yet been associated with these viruses. Plasmid DNA vaccines elicit potent and protective immune responses in numerous small-animal models of infectious diseases. However, their immunogenicity in primates appears less potent. In the United States, HTLV-I/II seroprevalence rates among volunteer blood donors average 0.016 percent. Approximately half of HTLV-I/II-seropositive blood donors nationwide are infected with HTLV-I. HTLV-I infected donors most often report a history of birth in HTLV-I endemic countries or sexual contact with persons from the Caribbean or Japan. In the past two decades a large initiative has been put forth to understand the biological and pathogenic properties of the human T-cell lymphotropic virus type 1 (HTLV-1); this has ultimately led to the development of various experimental vaccination and therapeutic strategies to combat HTLV-1 infection. These strategies include the development of envelope glycoprotein derived B-cell epitopes for the induction of neutralizing antibodies, as well as a strategy to generate a multivalent cytotoxic T-lymphocyte (CTL) response against the HTLV-1 Tax antigen. A vaccine candidate that can elicit or boost anti-gp46 neutralizing antibody response may have a potential for prevention and therapy against HTLV-1 infection.[17] Potential treatments include prosultiamine, a vitamin B-1 derivative, which has been shown to reduce viral load and symptoms;[18]azacytidine, an anti-metabolite, which has been credited with the cure of a patient in Greece;[19]tenofovir disoproxil fumarate (TDF), a reverse-transcriptase inhibitor used for HIV, and phosphonated carbocyclic 2'-oxa-3'aza nucleosides (PCOANs).[20] A newer formulation of TDF, called tenofovir alafenamide fumarate (TAF), also has promise as a treatment with less toxicity.